Abstract：
:In humans, action errors and perceptual novelty elicit activity in a shared frontostriatal brain network, allowing them to adapt their ongoing behavior to such unexpected action outcomes. Healthy and pathologic aging reduces the integrity of white matter pathways that connect individual hubs of such networks and can impair the associated cognitive functions. Here, we investigated whether structural disconnection within this network because of small-vessel disease impairs the neural processes that subserve motor slowing after errors and novelty (post-error slowing, PES; post-novel slowing, PNS). Participants with intact frontostriatal circuitry showed increased right-lateralized beta-band (12-24 Hz) synchrony between frontocentral and frontolateral electrode sites in the electroencephalogram after errors and novelty, indexing increased neural communication. Importantly, this synchrony correlated with PES and PNS across participants. Furthermore, such synchrony was reduced in participants with frontostriatal white matter damage, in line with reduced PES and PNS. The results demonstrate that behavioral change after errors and novelty result from coordinated neural activity across a frontostriatal brain network and that such cognitive control is impaired by reduced white matter integrity.
journal_name
Neurobiol Agingjournal_title
Neurobiology of agingauthors
Wessel JR,Ullsperger M,Obrig H,Villringer A,Quinque E,Schroeter ML,Bretschneider KJ,Arelin K,Roggenhofer E,Frisch S,Klein TAdoi
10.1016/j.neurobiolaging.2015.10.014subject
Has Abstractpub_date
2016-02-01 00:00:00pages
205-213eissn
0197-4580issn
1558-1497pii
S0197-4580(15)00518-7journal_volume
38pub_type
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journal_title：Neurobiology of aging
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journal_title：Neurobiology of aging
pub_type： 杂志文章
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